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Changes to the lateral geniculate nucleus in Alzheimer's disease but not dementia with Lewy bodies

Lookup NU author(s): Dr Daniel ErskineORCiD, Professor John-Paul TaylorORCiD, Dr Michael FirbankORCiD, Professor John O'Brien, Professor Ian McKeith, Professor Johannes Attems, Professor Alan ThomasORCiD, Dr Christopher Morris, Dr Ahmad Khundakar

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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND).


Abstract

AbstractAIMS:Complex visual hallucinations occur in 70% of dementia with Lewy bodies (DLB) cases and significantly affect patient well-being. Visuo-cortical and retinal abnormalities have been recorded in DLB and may play a role in visual hallucinations. The present study aimed to investigate the lateral geniculate nucleus (LGN), a visual relay centre between the retina and visual cortex, to see if changes to this structure underlie visual hallucinations in DLB.METHODS:Fifty-one [17 probable DLB, 19 control and 15 probable Alzheimer's disease (AD)] cases were recruited for a functional magnetic resonance imaging study, in which patients' response to a flashing checkerboard stimulus was detected and measured in the LGN, before comparison across experimental groups. Additionally, post mortem LGN tissue was acquired for a cross-sectional study using 20 (six DLB, seven control and seven AD) cases and analysed using stereology. α-Synuclein, phosphorylated tau and amyloid-β pathology was also assessed in all cases.RESULTS:DLB cases did not significantly differ from controls on neuroimaging, morphometry or pathology. However, a significant increase in amyloid-β pathology, a reduction in number of parvocellular neurones and magnocellular gliosis was found in AD cases compared with control and DLB cases.CONCLUSIONS:These findings suggest that the early visual system is relatively spared in DLB, which implies that upstream visual structures may be largely responsible for the generation of hallucinatory percepts. The significance of the degeneration of the LGN in AD cases is uncertain.


Publication metadata

Author(s): Erskine D, Taylor JP, Firbank MJ, Patterson L, Onofrj M, O'Brien JT, McKeith IG, Attems J, Thomas AJ, Morris CM, Khundakar AA

Publication type: Article

Publication status: Published

Journal: Neuropathology and Applied Neurobiology

Year: 2015

Volume: 42

Issue: 4

Pages: 366–376

Print publication date: 01/06/2016

Online publication date: 02/06/2015

Acceptance date: 06/05/2015

Date deposited: 23/09/2015

ISSN (print): 0305-1846

ISSN (electronic): 1365-2990

Publisher: Wiley-Blackwell Publishing Ltd.

URL: http://dx.doi.org/10.1111/nan.12249

DOI: 10.1111/nan.12249

PubMed id: 25967384


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Funding

Funder referenceFunder name
Alzheimer's Research UK
NHS National Institute of Health Research Biomedical Research Unit for Lewy body dementia, from the Yvonne Emily Mairy bequest
NIHR Newcastle Biomedical Research Centre and Unit
Wellcome Trust
Alzheimer's Society
NHS National Institute of Health Research Biomedical Research Unit for Lewy body dementia
G0400074UK Medical Research Council

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